B. juncea is grown in many countries of the world for the production of mustard and edible oil. Mustard quality genotypes of B. juncea are high in glucosinolate and erucic acid content. Some genotypes have been developed which are low in glucosinolate and erucic acid content, these are referred to as “canola quality” and are preferred for edible oil consumption. Brassica napus and B. rapa are other Brassica species that have been developed to produce canola oil. To be classified as canola, genotypes must have an erucic acid content of less than two percent in the oil and a glucosinolate content of less than 30 micromoles per gram of meal.
The genetic relationship among the Brassica species was described by U (1935). There are three diploid species, with the genome of B. rapa designated as ‘A’, the genome of B. nigra designated as ‘B’ and the genome of B. oleracea designated as ‘C’. There are three allotetraploid species in which the diploid genomes are combined. Thus, B. juncea has an AB genomic constitution by combining the genomes of B. rapa and B. nigra, B. napus has AC from B. rapa and B. oleracea, and B. carinata has BC from B. nigra and B. oleracea. During meiosis, the chromosomes from each genome will pair with their homologues, thus in B. juncea, A chromosomes will pair with A and B will pair with B. Interspecific crosses can be made between Brassica species, but progeny of the cross will be sterile. In a cross between B. juncea and B. napus, for example, the common A chromosomes will pair, but the B and C chromosomes will not pair well, causing sterility. Crossing back to either species can restore fertility, but the alien genome chromosomes are lost. For this reason, it is very difficult to get genetic transfer between chromosomes of different genomes, for example from the C genome of B. napus to the B genome of B. juncea. 
The allotetraploid species have homologous genes on the two genomes. For example, acetohydroxy acid synthase (AHAS), the first enzyme in the synthesis of the amino acids leucine, isoleucine and valine, is encoded by multiple gene members of a small gene family that are designated as AHAS genes. Rutledge et al. (Mol Gen Genet 229: 31-40, 1991) characterized the AHAS genes in B. napus. They found five AHAS genes, with AHAS2, AHAS3 and AHAS4 on the A genome and with AHAS1 and AHAS5 on the C genome. AHAS1 and AHAS3 are 98% homologous within their coding regions. Gene expression analysis by Ouellet et al., (Plant J. 2: 321-330, 1992) indicated that AHAS1 and AHAS3 are expressed at all growth stages and are the most important for normal growth. AHAS2 is active only in mature ovules and extra-embryonic tissues of immature seeds. AHAS4 and AHAS5 are not expressed in B. napus. 
Herbicide tolerance is a desired attribute in commercial varieties of the Brassica genus including B. napus, B. rapa and B. juncea. Herbicide tolerance provides an economically viable method to control a wide range of weeds in the crop. Weeds such as stinkweed, wild mustard, flixweed, ball mustard and shepard's purse are closely related to B. juncea and therefore difficult to control with herbicides without damaging the crop. With an herbicide tolerant variety, it is possible to control other varieties of the same species which do not possess the trait and thereby keep the variety pure. Imidazolinone herbicides affect amino acid biosynthesis in susceptible plants by disrupting activity of the AHAS enzyme. Resistance to imidazolinone herbicides has been developed in B. napus varieties of canola. Mutations in the AHAS coding regions alter the enzyme structure and prevent inhibition of the enzyme by the herbicide. Swanson et al. (Plant Cell Rep 7:83-87, 1988) reported the discovery of B. napus plants with mutations conferring tolerance to imidazolinone and sulfonylurea herbicides. Through sequence analysis, the mutation responsible for resistance to imidazolinones was identified as a single basepair change (G to A) in the 3′ end of the AHAS gene of the Arabidopsis mutant imr1, which caused an amino acid change from Ser to Asn (Sathasivan et al., Plant Physiol. 97:1044-1050, 1991; Hattori et al., Mol. Gen. Genet. 232: 167-173, 1992). In Brassica napus, the mutation responsible for resistance to multiple herbicides, including the imidazolinones, was identified as a single basepair change (G to T) in the 3′ end of AHAS3 causing an amino acid change from Trp to Leu (Hattori et al., Mol. Gen. Genet. 246: 419-425,1995).
Gingera et al. (U.S. Pat. No. 6,613,963) disclose three B. juncea lines with tolerance to imidazolinone herbicides derived from an interspecific cross between B. juncea and a tolerant B. napus variety, followed by three backcrosses to B. juncea. It is disclosed that the plants were tolerant to herbicide applied at the usual field rate. No molecular information is provided regarding how many mutated B. napus genes were actually transferred and, if both mutated genes transferred, where they are located in the B. juncea genomes. Since B. juncea and B. napus share the A genome, it would presumably be simple to transfer the mutated AHAS3 gene located on the A genome. It will be much more difficult to transfer the mutant AHAS1 gene from the C genome of B. napus to the B genome of B. juncea. When backcrossing to B. juncea, there will be a tendency to have B genome chromosomes replace the C chromosomes and thus the mutated AHAS1 gene will be lost. Selection for herbicide tolerance was carried out at each stage, but according to Swanson et al. (Theor Appl Genet 78:525-530,1989), the mutated AHAS3 gene on the A genome alone will provide tolerance to the usual field rate of herbicide. Thus, without the type of molecular information regarding the B. juncea AHAS gene sequences provided by this current invention, there would be no way to confirm that the mutated AHAS1 gene from B. napus was successfully transferred to B. juncea. While the mutated AHAS1 and AHAS3 genes together will act additively to provide enhanced tolerance to imidazolinone herbicides (Swanson et al., Theor Appl Genet 78:525-530, 1989), this will not be apparent at the herbicide rate disclosed by Gingera et al.
There remains a need for a B. juncea variety with a mutation in the AHAS1 gene on the B genome and a method to identify plants containing the mutant allele, especially in plants which already have a mutated AHAS3 gene. In this invention, we disclose information regarding creation of imidazolinone resistant B. juncea line J04E-0044, deposited as ATCC Accession Number PTA-6324, the mutant AHAS gene allele on the B genome of B. juncea line J04E-0044 (BjAHAS-bR) and selection methods for determining the presence of the mutant allele. It is obvious that the mutant allele of the B genome AHAS gene (BjAHAS-bR) is more likely to be stable than the AHAS1 mutant allele introgressed from B. napus. 